grant
Regulation of Nutrient Homeostasis by COMMD proteins
Organization UT SOUTHWESTERN MEDICAL CENTERLocation DALLAS, UNITED STATESPosted 1 Aug 2016Deadline 28 Feb 2031
NIHUS FederalResearch GrantFY2026ATP phosphohydrolaseATP7BATPaseAdenosine TriphosphataseAffectAgreementAnemiaAnimal ModelAnimal Models and Related StudiesAnimalsApicalAssayAutoregulationBackBile TractBiliaryBiliary SystemBiliary TreeBindingBinding ProteinsBioassayBiochemicalBiological AssayBiologyBrainBrain Nervous SystemCURLCanine SpeciesCanis familiarisCell BodyCell membraneCell surfaceCellsCerebral PseudosclerosisClosure by LigationCompartment of the Uncoupling Receptors and LigandsComplexCopperCopper-transporting ATPase 2Cu elementCytoplasmic MembraneDNA mutationDataDefectDockingDogsDogs MammalsDorsumEarly EndosomeEncephalonEndosomesEnzyme GeneEnzymesEquilibriumEventExcretory functionExocytosisFundingGTPGenesGenetic ChangeGenetic defectGenetic mutationGowers' choreaGrantGuanosine TriphosphateHepatic CirrhosisHepato-Neurologic Wilson DiseaseHepatocerebral DegenerationHepatolenticular DegenerationHomeostasisHypomelanosisHypopigmentationImmune DiseasesImmune DisordersImmune DysfunctionImmune System DiseasesImmune System DisorderImmune System DysfunctionImmune System and Related DisordersImmunologic DiseasesImmunological DiseasesImmunological DysfunctionImmunological System DysfunctionImpairmentIn VitroIntermediary MetabolismIntestinalIntestinesKO miceKinnier-Wilson DiseaseKnock-out MiceKnockout MiceKnowledgeLeadLigand Binding ProteinLigand Binding Protein GeneLigationLiverLiver CirrhosisLocationLysosomesMediatingMembrane Protein GeneMembrane ProteinsMembrane-Associated ProteinsMetabolic ProcessesMetabolismMethodsMiceMice MammalsMolecularMolecular InteractionMonomeric G-ProteinsMonomeric GTP-Binding ProteinsMovementMurineMusMutationNerve DegenerationNervous System InjuriesNervous System TraumaNervous System damageNeurohepatic DegenerationNeurological DamageNeurological InjuryNeurological traumaNeuron DegenerationNull MouseNutrientNutritionOrganOrganellesPathway interactionsPb elementPhysiologicPhysiologicalPhysiological HomeostasisPlasma MembranePlayProcessProgressive Lenticular DegenerationProtein BindingProtein TraffickingProteinsPseudosclerosisPublicationsReceptosomesRecyclingRegulationReportingRoleRouteScientific PublicationSmall G-ProteinsSmall GTPasesSmall IntestinesSurface ProteinsSystemTestingVesicleWestphal Strumpell diseaseWestphal pseudosclerosisWestphal-Strumpell SyndromeWilson DiseaseWilson disease Cu-binding P type ATPaseWilson disease proteinWorkabsorptionbalancebalance functionbariatric surgerybiliary tractbody movementbound proteinbowelcaninedomestic dogexcretionexperimentexperimental researchexperimental studyexperimentsextracellularfamilial hepatitisgastric bandinggastric bypass surgerygenome mutationheavy metal Pbheavy metal leadhepatic body systemhepatic organ systemimplantable gastric stimulation bandingin vivoinjury to tissueinterestlate endosomeleukodermaloss of function mutationmodel of animalmouse modelmurine modelneural degenerationneurodegenerationneurodegenerativeneurological degenerationneuronal degenerationneurotraumanutrient absorptionnutrient requirementobesity surgerypathwayplasmalemmaprotein transportresponsesmall bowelsocial rolestomach staplingtissue injurytraffickingtrans-Golgi Networkweight loss surgery
Description preview
PROJECT SUMMARY
Copper (Cu) is a vital nutrient required by many essential enzymes. Cu-transporting ATPases, ATP7A and
ATP7B, play pivotal roles in delivering Cu to proteins in the secretory pathway or to vesicles that mediate
extracellular excretion of Cu. In response to varying levels in cellular Cu, ATP7A and B undergo dynamic
movement between…
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